Averill D B, Diz D I
Hypertension and Vascular Disease Center, Wake Forest University School of Medicine, Winston-Salem, NC 27157, USA.
Brain Res Bull. 2000 Jan 15;51(2):119-28. doi: 10.1016/s0361-9230(99)00237-3.
The baroreceptor reflex is a relatively high gain control system that maintains arterial pressure within normal limits. To a large extent, this is accomplished through central neural pathways responsible for autonomic outflow residing in the medulla oblongata. The circulating renin-angiotensin system also contributes to the regulation of blood pressure, predominantly through its effects on the control of hydromineral balance and fluid volume. All the components of the renin-angiotensin system are also found in the brain. One of the principal products of the renin-angiotensin system cascade (brain or blood), angiotensin II, modulates the baroreceptor reflex by diminishing the sensitivity of the reflex and shifting the operating point for regulation of sympathetic outflow to higher blood pressures. This paper reviews our current knowledge about the neuronal pathways in the medulla oblongata through which angiotensin peptides alter the baroreceptor reflex control of sympathetic nerve activity. Emphasis is placed on the probable components and neural mechanisms of the medullary baroreflex arc that account for the ability of angiotensin peptides to change the sensitivity of the baroreceptor reflex and to shift the baroreceptor reflex control of sympathetic outflow to higher blood pressures in a pressure-independent manner.
压力感受器反射是一个相对高增益的控制系统,可将动脉血压维持在正常范围内。在很大程度上,这是通过位于延髓内负责自主神经输出的中枢神经通路来实现的。循环中的肾素-血管紧张素系统也有助于血压调节,主要是通过其对水盐平衡和血容量控制的影响。肾素-血管紧张素系统的所有成分在大脑中也都有发现。肾素-血管紧张素系统级联反应(脑内或血液中)的主要产物之一——血管紧张素II,通过降低反射敏感性并将交感神经输出调节的工作点转移到更高血压水平来调节压力感受器反射。本文综述了我们目前对延髓中神经通路的认识,通过这些通路,血管紧张素肽改变压力感受器对交感神经活动的反射控制。重点在于髓质压力反射弧可能的组成部分和神经机制,这些机制解释了血管紧张素肽改变压力感受器反射敏感性以及以压力非依赖性方式将压力感受器对交感神经输出的反射控制转移到更高血压水平的能力。